Item request has been placed!
×
Item request cannot be made.
×
Processing Request
Interfering with hyaluronic acid metabolism suppresses glioma cell proliferation by regulating autophagy.
Item request has been placed!
×
Item request cannot be made.
×
Processing Request
- Additional Information
- Source:
Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101524092 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-4889 (Electronic) NLM ISO Abbreviation: Cell Death Dis Subsets: MEDLINE
- Publication Information:
Original Publication: London : Nature Pub. Group
- Subject Terms:
- Abstract:
The tumor microenvironment plays an important role in tumor progression. Hyaluronic acid (HA), an important component of the extracellular matrix in the tumor microenvironment, abnormally accumulates in a variety of tumors. However, the role of abnormal HA accumulation in glioma remains unclear. The present study indicated that HA, hyaluronic acid synthase 3 (HAS3), and a receptor of HA named CD44 were expressed at high levels in human glioma tissues and negatively correlated with the prognosis of patients with glioma. Silencing HAS3 expression or blocking CD44 inhibited glioma cell proliferation in vitro and in vivo. The underlying mechanism was attributed to the inhibition of autophagy flux and maintaining glioma cell cycle arrest in G1 phase. More importantly, 4-methylumbelliferone (4-MU), a small competitive inhibitor of Uridine diphosphate (UDP) with the ability to penetrate the blood-brain barrier (BBB), also inhibited glioma cell proliferation in vitro and in vivo. Thus, approaches that interfere with HA metabolism by altering the expression of HAS3 and CD44 and the administration of 4-MU potentially represent effective strategies for glioma treatment.
- References:
Matrix Biol. 2019 May;78-79:118-138. (PMID: 29673760)
Adv Cancer Res. 2014;123:35-65. (PMID: 25081525)
Cell Death Dis. 2018 Oct 9;9(10):1032. (PMID: 30302016)
Pancreas. 2017 Feb;46(2):190-197. (PMID: 27846148)
Adv Cancer Res. 2014;123:95-119. (PMID: 25081527)
J Biol Chem. 2007 Jul 6;282(27):19426-41. (PMID: 17493932)
Nat Rev Cancer. 2020 Jan;20(1):57-70. (PMID: 31806884)
Cancers (Basel). 2018 Dec 03;10(12):. (PMID: 30513961)
Int J Mol Sci. 2019 Feb 15;20(4):. (PMID: 30781344)
J Biochem. 2013 Nov;154(5):395-408. (PMID: 24092768)
Toxins (Basel). 2013 Oct 17;5(10):1814-26. (PMID: 24141285)
Proc Natl Acad Sci U S A. 2018 May 29;115(22):5768-5773. (PMID: 29760085)
Adv Drug Deliv Rev. 2016 Feb 1;97:186-203. (PMID: 26541745)
J Clin Neurosci. 2016 Dec;34:1-5. (PMID: 27578526)
Autophagy. 2016 Oct 2;12(10):1954-1955. (PMID: 27485905)
Front Immunol. 2015 Mar 23;6:123. (PMID: 25852691)
Autophagy. 2018;14(11):2007-2022. (PMID: 30025493)
Int J Cancer. 2007 Jun 15;120(12):2557-67. (PMID: 17315194)
Clin Cancer Res. 2009 Sep 1;15(17):5308-16. (PMID: 19706824)
Autophagy. 2018;14(9):1481-1498. (PMID: 29956571)
Autophagy. 2013 May;9(5):714-29. (PMID: 23519090)
J Natl Cancer Inst. 2015 Apr 13;107(7):. (PMID: 25868577)
Semin Cancer Biol. 2008 Aug;18(4):288-95. (PMID: 18468453)
Cell Metab. 2017 May 2;25(5):1037-1043. (PMID: 28467923)
Adv Cancer Res. 2014;123:231-54. (PMID: 25081532)
Physiol Rev. 2011 Jan;91(1):221-64. (PMID: 21248167)
Mol Diagn Ther. 2015 Oct;19(5):299-308. (PMID: 26232909)
Cancer Cell. 2012 Mar 20;21(3):309-22. (PMID: 22439926)
J Cell Biol. 1994 Jul;126(2):391-401. (PMID: 7518464)
Carbohydr Polym. 2016 Oct 5;150:139-48. (PMID: 27312623)
Clin Transl Immunology. 2015 Dec 04;4(12):e52. (PMID: 26719798)
J Biol Chem. 2014 Aug 15;289(33):22888-22899. (PMID: 24973214)
Cancer Lett. 2016 May 28;375(1):20-30. (PMID: 26921785)
Semin Cancer Biol. 2020 Nov;66:12-21. (PMID: 31319163)
Nat Commun. 2020 Sep 16;11(1):4660. (PMID: 32938908)
- Accession Number:
9004-61-9 (Hyaluronic Acid)
- Publication Date:
Date Created: 20210514 Date Completed: 20211014 Latest Revision: 20211014
- Publication Date:
20250114
- Accession Number:
PMC8119697
- Accession Number:
10.1038/s41419-021-03747-z
- Accession Number:
33986244
No Comments.